Anxiety is a natural reaction to stress that quickly heightens awareness for an individual during a dangerous situation, which has a potential survival benefit. Many individuals are able to reduce or extinguish the anxiety after the danger is over and return to a normal baseline state. Individuals with excessive anxiety may have difficulty controlling their anxiety, and this can have a deleterious effect on their quality of life. People with anxiety disorders can have an amplification of the anxiety response every time they experience the trigger or an approximation of the trigger. Of the main types of anxiety disorders—social anxiety disorders, panic disorders, phobias, and generalized anxiety disorder—generalized anxiety lacks a specific cause while the other disorders have a purported if not known cause. Treating these anxiety disorders can be difficult because each type requires different treatments and therapeutic approaches. Additionally, fear and anxiety are tied with a strong memory network. In order to treat these disorders, reintroduction of a neutral quality to stimuli that may have become associated with trauma is typically required.
Many previous studies have implicated the amygdala as the brain structure involved in many anxiety phenotypes, in both human and mouse models and as a mediator of the emotional output of fear and anxiety. Hyperexcitability and hyperactivity are key features of anxiety disorders. Inputs from many brain regions converge on the amygdala to allow an individual to judge the true danger of a situation and create the proper response. Significant links between the amygdala and fear-based memory could explain why traumatic events may appear to be encoded for a longer period than might be adaptive or helpful to the individual. Manipulating the emotional charge to traumatizing stimuli could potentially alter the inappropriate response.
Current prescribed medications deliver an instant, but not long lasting, relief of anxiety through their sedative, anxiolytic, and relaxant properties. There is evidence that anxious patients may try to self-medicate through the intake of nicotine, although differential responsiveness to the effects of nicotine may blunt this effect. A specific nicotinic acetylcholine receptor subtype (nAChRs), α7, has been implicated in regulating the network excitability of the amygdala. Cholinergic modulation, therefore, is a factor for the investigation of anxiolytic strategies. The cholinergic system plays a role in many facets of brain function, including learning and memory and plasticity. A consideration of long-term effects of cholinergic modulation, including plasticity mechanisms, may be informative to our understanding of anxiety mechanisms.